| Summary: | 碩士 === 國立中興大學 === 獸醫學系暨研究所 === 101 === Cushing’s syndrome refers to the clinical manifestations induced by chronic exposure to excess endogenous or exogenous glucocorticoids. The cause of Cushing’s syndrome could be classified into adrenocorticotropic hormone (ACTH)-dependent and ACTH-independent, in which ACTH-dependent is the most common cause of spontaneous Cushing’s syndrome in humans and canines. Trivalent chromium (Cr3+) is not only an essential element for animals, it is also widely studied for its clinical use because of its variety of beneficial biological functions. Based on studies, we postulated that Cr3+ could be helpful on attenuating ACTH-dependent Cushing’s syndrome by decreasing the level of glucocorticoids. In this study, rats were randomly divided into four groups: (1) rats treatment of placebo and saline were taken as control group; (2) rats treatment of Cr3+ and saline were taken as Cr group; (3) rats treatment of placebo and ACTH were taken as ACTH group; (4) rats treatment of Cr3+ and ACTH were taken as ACTH with Cr group. After treatment for 28 days, all rats were sacrificed with humanism. The body weights every week , tissues weights, the levels of corticosterone, AST, ALT, ALP at the 28th day were measured, and histological examination of the adrenal gland and liver were observed. The results showed that Cr3+ supplementation in ACTH-stimulated rats decreased the levels of corticosterone, AST, ALT, ALP in comparison to ACTH-stimulated rats without Cr3+ supplementation. In addition, the histological examination showed the cells and lipid droplets in the zona fasciculata and the zona reticularis in the adrenal gland were smaller and fewer, and vacuoles in the hepatic cells were fewer in ACTH-stimulated rats with Cr3+ supplementation than that in ACTH-stimulated rats without Cr3+ supplementation. Taken up together, Cr3+ administration had an inhibitory effect on the secretion of corticosterone by adrenal gland in ACTH-stimulated rats and attenuated the hepatic damage caused by glucocorticoids excess.
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